Two stimuli for thirst are now recognized. The first, osmoregulatory thirst, is believed to be mediated by osmoreceptors in the lateral preoptic area (LPO), in part because LPO lesions abolish water ingestion during a 4-hr test following the IP injection of hypertonic NaCl solution. However, we have found that lesioned animals increase their water intakes when tests are prolonged to 24 hr, when NaCl is given in their diet, and when NaCl is administered IV. These and other findings raise new doubts about the role of the LPO in thirst produced by administration of osmotic loads. The second stimulus for thirst, hypovolemia, is believed to be mediated, in part, by the renin-angiotensin system. However, we find that the plasma renin activities produced by various treatments which elicit thirst do not account for more than 20% of the observed drinking behavior. Furthermore, we find that nephrectomy reduces water intake following these treatments by removing the pressor function of angiotensin and thereby undermining the capacity of the animals to behave, rather than by removing a specific dipsogenic stimulus. These results suggest that the renin-angiotensin system is not largely responsible for the drinking elicited in rats by acute hypovolemia or hypotension.